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Sox9 directs hypertrophic maturation and blocks osteoblast differentiation of growth plate chondrocytes

Peter Dy1, Weihuan Wang, Pallavi Bhattaram

  • 1Department of Cell Biology, Orthopaedic and Rheumatologic Research Center, Cleveland Clinic Lerner Research Institute, Cleveland, OH 44195, USA.

Developmental Cell
|March 17, 2012
PubMed

Insights

The transcription factor Sox9 is crucial for maintaining chondrocyte proliferation and hypertrophy in the growth plate. This research clarifies Sox9

Area of Science:

  • Skeletal Biology and Musculoskeletal Diseases
  • Developmental Biology
  • Cellular and Molecular Biology

Background:

  • The transcription factor Sox9 is essential for early chondrogenesis (cartilage formation).
  • Its later roles in the cartilage growth plate, vital for skeletal growth and endochondral ossification, are not well understood.

Purpose of the Study:

  • To investigate the function of Sox9 in maintaining the structure and differentiation of the postnatal growth plate.
  • To elucidate the molecular mechanisms by which Sox9 regulates chondrocyte proliferation, hypertrophy, and lineage progression.

Main Methods:

  • Utilized a doxycycline-inducible Cre-lox system in mice with conditional Sox9 null alleles.
  • Analyzed gene expression (Runx2, Col10a1), signaling pathways (β-catenin), and cellular phenotypes in growth plate chondrocytes.

Main Results:

  • Sox9 is required for sustained chondrocyte columnar proliferation and the induction of cell hypertrophy in the growth plate.
  • Sox9 suppresses Runx2 expression and β-catenin signaling, preventing premature progression to prehypertrophy and osteoblastic differentiation.
  • Sox9 protein persists longer than its RNA in hypertrophic chondrocytes, where it collaborates with Mef2c to activate Col10a1 expression.

Conclusions:

  • Sox9 remains a critical regulator of chondrocyte lineage fate and differentiation throughout the multistep process in the growth plate.
  • These findings provide key molecular insights into skeletogenesis and the regulation of cartilage development and maintenance.

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